Investigations
1st investigations to order
bedside cognitive testing
Test
Tools include the Folstein Mini-Mental State Examination (MMSE), the most commonly used screening test (with high sensitivity for detecting dementia, but which often fails to recognise mild cognitive impairment [MCI]), and the Blessed Dementia Scale.[92]
Several other tools are available for bedside screening (e.g., the Saint Louis University Mental Status [SLUMS] examination, and Mini-Cog). Saint Louis University School of Medicine: SLUMS Examination Opens in new window Alzheimer's Association: Mini-Cog(TM) Opens in new window
The SLUMS examination has better sensitivity for detecting MCI than the MMSE.[93] The SLUMS examination also accounts for educational background when stratifying cognitive functioning, which will become increasingly important as the sensitivity and specificity of early diagnosis is refined.
Meta-analyses indicate that the Mini-Cog may be a useful cognitive screening tool.[92][94]
Alzheimer's Association: Mini-Cog(TM)
Opens in new window However, only a limited number of diagnostic studies using Mini‐Cog are available.[92][94]
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The Montreal Cognitive Assessment (MoCA) test can be used to detect MCI.[68] Montreal Cognitive Assessment Opens in new window
Result
impaired recall, nominal dysphasia, disorientation (to time, place, and eventually person), constructional dyspraxia, and impaired executive functioning
FBC
Test
Result
to rule out anaemia
metabolic panel
Test
Hypo- or hypernatraemia, hypo- or hypercalcaemia, and hypo- or hyperglycaemia should be sought to rule out metabolic causes of dementia.
Result
to exclude abnormal sodium, calcium, glucose levels
serum thyroid-stimulating hormone (TSH)
Test
Rule out hyperthyroid- or hypothyroid-associated dementia.
Result
TSH may be low or high
serum vitamin B12
Test
Rule out vitamin B12 deficiency-induced dementia.
Result
may be low
urine drug screen
Test
Rule out recreational drug use.
Result
may be positive
CT
Test
Useful in excluding tumours, normal pressure hydrocephalus, subdural haematoma, or vascular disease. In early AD, few changes are evident, although pronounced sulcal/gyral changes and global atrophy may be evident later in the disease.
Structural imaging is recommended at least once during the work-up.[75][76]
Result
may exclude space-occupying lesions or other pathology
Investigations to consider
cerebrospinal fluid (CSF) analysis
Test
Not routinely required, but may rule out infectious causes of dementia, particularly in younger people.
A 2017 Cochrane review concluded that there is some continued uncertainty regarding the value of CSF biomarker measurement (total tau, phosphorylated tau [p‐tau], or p‐tau/ABeta ratio) for identifying which people with mild cognitive impairment will develop the diagnosis of AD within a specified period.[71] However, a combination of low ABeta-1-42 and elevated tau or p-tau shows high diagnostic specificity in the context of cognitive changes.[72][73][74]
Result
may show evidence of infectious aetiology for dementia; biomarker testing may show patterns of Abeta and p-tau that may be suggestive of AD as the aetiology of the dementia
serum rapid plasma reagin/Venereal Disease Research Laboratory (VDRL)
Test
Rules out syphilis as a cause of dementia in people at risk.
Result
may be positive
serum HIV
Test
Rules out HIV infection as a cause of dementia in people at risk.
Result
may be positive
formal neuropsychological testing
Test
Sometimes helpful in differentiating between normal ageing, mild cognitive impairment, and early AD, as well as differentiating other neurodegenerative dementias such as dementia with Lewy bodies or frontotemporal dementia.
Batteries include: Wechsler's tests for intellectual functioning; Boston naming test for language processing; semantic and category fluency (FAS and animal naming); Rey-Ostrich Complex Figure test for visuo-spatial processing; digit span and reverse/trail making test for attention and memory; Wisconsin card sorting test and Trails B for executive functioning.
Result
delayed verbal recall; impaired memory; visuo-spatial abnormalities; difficulties naming objects
genetic testing
Test
Offered in early onset dementia or when a strong family history is present.[70]
Result
chromosome 1, 14, 21 mutations
fluorodeoxyglucose-PET (FDG-PET)
Test
Localises areas of greatest brain involvement.
Fluorodeoxyglucose (FDG)-PET can distinguish patients with AD from people without AD, and shows characteristic reductions of regional glucose metabolic rates in patients with probable and definite AD.[87] Particularly useful in atypical presentations when imaging results are likely to impact patient care.[88][89]
Result
decreased glucose uptake in pattern specific to AD
single-photon emission CT (SPECT)
Test
SPECT with Tc-99m hexamethylpropyleneamine oxime (HMPAO) shows bilateral temporoparietal hypoperfusion in patients with AD. These changes can occur early in the disease process and may help distinguish AD from other forms of dementia.[90]
Not universally available and rarely required.[76]
Result
decreased perfusion of temporal lobes
electroencephalogram (EEG)
Test
Not recommended as a first-line diagnostic tool. Slowing of rhythm is more marked in Lewy body dementia than in AD.[91]
EEG has characteristic features in Creutzfeld-Jacob disease and should be sought when temporal lobe signs, other seizure phenomena, or a clinical history suggestive of transient epileptic amnesia are present.
Result
transient generalised slowing of rhythm
Emerging tests
amyloid-PET
Test
Identifies regions of amyloid-beta deposition using a radio-ligand superimposed on structural brain imaging. PET scans using amyloid-binding ligands show promise in identifying people with mild cognitive impairment who are likely to develop AD.[81][82][83] Can also be helpful in complicated cases to differentiate dementia aetiologies.[85][95]
Currently, amyloid PET imaging is primarily used in the research setting or in the evaluation of unusual presentations.
Result
evidence of presumably pathological amyloid-beta deposition
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